Valvular Heart Disease 1 Flashcards
1
Q
Right atrium and Right ventricle separated by
A
tricuspid valve
2
Q
Right ventricle connected to pulmonary artery through
A
pulmonary semilunar valve
3
Q
Left atrium connected to left ventricle by
A
mitral (bicuspid) valve
4
Q
Left ventricle connected to aorta through
A
aortic semilunar valve
5
Q
valves are part of the
A
endocardium
6
Q
valves are covered by
A
endothelium
7
Q
The interior of valves is composed of
A
dense connective tissue containing fibroblasts, collagen and elastic fibers, and extracellular matrix
8
Q
How should valves look normally?
A
thin and nearly transparent
9
Q
What valves are open in systole?
A
pulmonic valve and aortic valve
10
Q
What valves are open in diastole?
A
mitral and tricuspid valve
11
Q
Aortic valve normal anatomy
A
3 cusps
right coronary cusp
non-coronary cusp
left coronary cusp
12
Q
Mitral valve normal anatomy
A
2 leaflets - anterior and posterior
2 papillary muscles (supply chordinae tendinae)
mitral valve orifice 4-6 cm^2
13
Q
Mitral valve leaflets
A
Each leaflet divided in 3 segments
Anterior leaflet = A1, A2, A3
Posterior leaflet = P1, P2, P3
14
Q
mark the joining of the leaflets
A
commisures
15
Q
commissures in the mitral valve
A
anterior commissure
posterior commissure
16
Q
what vascularizes the mitral valve
A
the coronary sinus and circumflex artery
17
Q
right heart valves
A
tricuspid valve - 3 leaflets (anterior, posterior, septal)
pulmonic valve
18
Q
Systole happens between (which heart sounds)
A
S1 and S2
19
Q
On physical exam, the 4 auscultatory sites are
A
Aortic area
Pulmonic area
Tricuspid area
Mitral area
20
Q
Intercostal space for aortic area on physical exam
A
btw. 2nd and 3rd intercostal
21
Q
Intercostal space for pulmonic area on physical exam
A
btw. 2nd and 3rd intercostal
22
Q
Intercostal space for tricuspid area on physical exam
A
btw. 4th and 5th intercostal
23
Q
Intercostal space for mitral area on physical exam
A
btw. 4th and 5th intercostal
24
Q
Normal findings on Physical exam
A
(1) Crisp S1 and S2
(2) Physiologic splitting of S2 (with inspiration, A2 then P2)
(2) No RV lift, PMI normal, JVP is 7cm H2O or less
(4) No diastolic murmur
(5) May have soft 2/6 “flow murmur” at left sternal border
25
On physical exam, hearing S3 may be normal in
children and young adults
26
Auscultatory findings (sounds)
Murmurs, Rubs, Clicks, Snaps
27
Murmur
turbulent flow (causes vibration)
in diastole or systole
can be from valvular disease or not
can be from stenosis or regurgitation
28
valvular stenosis
valve doesn't fully open
29
valvular regurgitation
valve doesn't fully close
30
Rub
scratchy, "squeaky leather" sound
from the rubbing of visceral and parietal pericardial layers
31
Systolic ejection click
high pitched sound of the aortic or pulmonic valve opening
occurs after S1 (systole)
32
systolic non-ejection click
high pitched sound of the closure of mitral valve
occurs after S1 (systole)
33
snap
short, high-frequency sound after S2 (diastole)
due to sudden arrest of the opening of mitral or tricuspid valve
34
mitral stenosis (MS) heard during
diastole
| after S2
35
aortic regurgitation (AR) heard during
diastole
| after S2
36
mitral regurgitation (MR) heard during
systole
| after S1
37
aortic stenosis (AS) heard during
systole
| after S1
38
Valvular Heart Diseases
```
Bicuspid aortic valve
Mitral valve prolapse
Rheumatic valvular heart disease
Infective endocarditis
Calcific valvular disease
Nonbacterial thrombotic endocarditis
Carcinoid tumor
```
39
Other causes of valvular heart disease
Trauma
Syphilis
Ankylosing spondylisis
Marfan's syndrome
40
Trauma (valvular heart disease)
ruptured papillary muscle
| ruptured chordae
41
Syphilis (valvular heart disease)
Dilated aortic root; aortic insufficiency
Invasion of the Treponema pallidum into the ascending aorta through the lymphatics leading to the destruction of elastic and connective tissue
42
Ankylosing Spondylisis
Chronic inflammatory disease in men affecting the spine and sacroiliac joints
associated with HLA-B27
chronic inflammation leads to fibrosis and endarteritis of the aortic root
43
Marfan's syndrome (valvular heart disease)
Aortic root dilation
| Mitral valve prolapse
44
Bicuspid aortic valve etiology
congenital fusion of 2 of the 3 cusps during development
+/- calcification of cusps develops w age
45
Bicuspid aortic valve
most commonly due to fusion of LCC and RCC
affects 2% population
runs in families
+/- stenosis, +/- regurgitation
many patients go undetected and ever need repair or replacement
46
Bicuspid aortic valve associated with
coarction of the aorta
Turner syndrome (45, X)
dilation of the ascending aorta
47
In bicuspid aortic valve, more likely to have
dilated ascending > descending aorta
more likely to rupture
need aortic aneurysm screening w CTA or MRA
repair ascending aorta at 5cm (or 4.5 cm if having another surgery)
48
Mitral valve prolapse (MVP) epidemiology
2%
| males > females
49
MVP etiology
genetic (AD)
| associated with Connective Tissue diseases (e.g. Marfan's)
50
MVP histopathology
Valve collagen + elastic fibers fragment
Myxomatous Connective Tissue accumulates
--> weakened leaflets stretch
--> prolapse/balloon into left atrium in systole
51
MVP associated with
infective endocarditis, palpitations, arrhythmias
52
MVP causes
mitral regurgitation
degree of regurgitation determines if surgery warranted
53
in MVP, the valve is repaired or replaced?
repaired
54
what is controversial about MVP?
controversial recommendation to take antibiotics propr to invasive procedures to help protect against infective endocarditis
(most recent guidelines say not indicated; most cardiologists still do it)
55
Rheumatic Heart Disease (RHD) epidemiology
children > adults
| uncommon in industrialized countries; common in developing countries
56
most common form of valvular heart disease worldwide
RHD (rheumatic heart disease)
57
RHD etiology
group A beta-hemolytic streptococcus (GAS)
58
RHD disease progression
3% strep pharyngitis infections ---(2-3 wks)--> Acute Rheumatic Fever (ARF)
can lead to chronic RHD (result of endocarditis/valvulitis)
59
Acute Rheumatic Fever results in
Pancarditis:
- Endocarditis/Valvulitis (can lead to Chronic RHD)
- Myocarditis (resolves)
- Pericarditis (resolves)
60
ARF diagnosis made by
Jones Criteria (5-15 years old)
need evidence of GAS infection and:
2 major or
1 major and 2 minor criteria
61
Major criteria for ARF diagnosis
JNES
```
Joint - migratory polyarthritis (carditis)
Nodules in skin (subcutaneous)
Erythema mardinatum (skin rash w advanced edging and clearing center)
Sydneham chorea (involuntary movements)
```
62
Minor criteria for ARF diagnosis
MFIR
Migratory arythralgias
Fever
Increased acute phase reactants (ESR, CRP, leukocytosis)
PRolonged PR interval on ECG
63
Evidence of streptococcal infection for diagnosis of ARF
```
antistreptolysin 0 (AS0) antibodies
Positive throat culture for GAS
```
64
RHD pathogenesis theory
GAS bacteria infect pharynx, skin, etc.
Antibodies develop to GAS M protein
Antibodies cross-react with heart tissues (type 2 autoimmune response)
Antibodies attack endocardium (valves, mitral > aortic > others), myocardium and pericardium
65
Valves in ARF
valves swollen, inflamed
| + small fibrin vegetations at edges
66
Myocardium in ARF
granulomas = Aschoff body
Macrophages in granulomas = Anischkow cells (with owl eye/caterpillar nuclei)
Degenerated collagen
67
Chronic RHD pathogenesis
repair with fibrosis
68
Chronic RHD valves
thickened with fibrosis
+/- fusion of neighbor leaflets/cusps
--> stiff valve
69
Chronic RHD - which valve affected?
mitral > aortic > others
70
Chronic RHD - chordae tendineae
thickened, shortened w fibrosis
71
Chronic RHD - how long to develop?
10-30 years
72
stenotic aortic valve with cup fusion
chronic RHD
73
cusp fusion; thickened, fibrotic mitral valve and chordae tendineae
chronic RHD
74
thickened, fibrotic, stenotic mitral valve lumen with leaflet fusion
chronic RHD
75
Infective endocarditis (IE) definition
infection of endocardium of heart, specifically the valves
76
IE etiology
bacteria >> others
77
IE - which valves affected?
mitral, aortic > others
78
IE - 2 types
Acute bacterial endocarditis
Subacute bacterial endocarditis (SBE)
79
Acute bacterial endocarditis
presents as an acute, fulminant infection
80
SBE
presents with a more insidious course
81
Acute Bacterial Endocarditis etiology
virulent organisms (e.g. staphylococcus aureus)
82
Acute Bacterial Endocarditis dx progression
normal heart valve
rapid progression
valve damage/necrosis
83
Acute Bacterial Endocarditis seen in
IV drug abusers
-when inject drug, innoculare with skin flora (Staph)
tricuspid valve (right heart) involved
84
SBE etiology
less virulent organisms (e.g. streptococci viridans)
85
SBE dx progression
abnormal heart valve (congenital, RHD, prosthetic)
insidious course
valve damage/necrosis LESS LIKELY
86
Acute and SBE pathogenesis
normal/abnormal valve injury
+/- injury
fibrin thrombus formation on valve (=vegetation)
transient bacteremia (detnal, OB, catheters, etc.)
bacteria adhere to and colonize fibrin thrombusa
acute inflammation
+/- necrosis of valve
87
Complications in Acute/SBE from fibrin thrombus formation (vegetation) +/- bacteria
embolize (septic emboli or aseptic emboli) -->
CNS, kidneys, spleen, skin, etc. -->
Infarcts and/or abscesses and/or hemorrhages (splinter, petechiae)
88
Acute/SBE complications
septic embolus in brain
splinter hemorrhage
splenic infarcts
petechiae in conjunctiva
89
IE cardiac lesions that predispose to endocarditis
anything that denudes endothelium off the surface of the heart
90
Characteristics of infecting organisms in IE
(1) have access to the bloodstream
(2) survive in the circulation
(3) adhere to the endocardium
91
Typical organisms in IE
- Staphylococci (S. aureus, Coag neg staph)
- Streptococci (viridans, enterococci, S. bovis, etc.)
- Culture Negative (HACEK)
92
Culture negative organisms in IE
rare, gram -, part of OP flora
```
H - haemophilus
A - aggregatibacter
C - cardiobacterium
E - eikenella
K - kingella
```
93
IE treatment
Prolonged IV and Oral antibiotics
Surgery to remove vegetations, abscesses or replace damaged valves
94
IE prevention
oral antibiotics given BEFORE procedures likely to produce bacteremia
in patients with conditions that predispose to IE
95
Calcific Valvular Disease (CVD) epidemiology
elderly (60s and 70s)
96
most common cause of acquired valvular disease in the developed world
CVD
97
CVD affects which valves?
left sided valves
98
CVD pathogenesis
develop due to wear and tear on valve
inflammation similar to pathogenesis of atherosclerosis
active calcification by a "osteoblast-like" cell
can develop on congenital bicuspid valve
99
CVD - valvue features
aortic/mitral valves with thickened, rigid, calcified cusps with calcified verrucae
100
CVD - commissures
normal commissures
101
CVD leads to
-aortic stenosis
(LVH and failure)
-mitral stenosis and regurgitation
(Pulmonary edema, pulm. HTN, A fib, HF)
102
CVD - treatment
valve replacement (only effective treatment)
103
Nonbacterial thrombotic endocarditis (NBTE) also known as
Marantic endocaditis
104
NBTE epidemiology
occurs in patients with "wasting diseases"
| i.e. cancer, adenoCA, blood; DIC, etc.
105
NBTE pathogenesis
? increased coagulability or ? Ag-Ab
106
NBTE - valve features
sterile fibrin vegetations
mitral and aortic valves
107
NBTE affects which valves
left sided valves
mitral and aortic valves
108
NBTE - complications
+/- embolize --> infarcts
109
Carcinoid tumor definition
malignancy of neuroendocrine cells (lung, GI tract) that produce abnormally high levels of serotonin
110
Carcinoid Tumor dx progression
serotonin induces fibrosis of the valvular endocardium of the right-sided valves -->
fibrosis causes thickening and restriction of the leaflets of the tricuspid and pulmonic valve -->
typically, leads to severe tricuspid regurgitation and severe pulmonic stenosis
111
Carcinoid tumor -which valves affected?
right-sided valves
